As a therapeutic agent for senile dementia, there have been mainly applied activators of cerebral circulation and metabolism, but these drugs have no improving effect on disintegration of the central nervous system which is believed to cause senile dementia. Consequently, they possess no improving effect on dysmnesia and acalculia which are said to be central symptoms of dementia. In view of the above, there has been desired a new therapeutic agent for senile dementia which promotes the repair and growth of nervous systems while inhibiting the disintegration of the central nervous system.
On the other hand, it was reported that apolipoprotein E may be generated at a high level at the sites of nervous systems which were damaged and are being repaired (For example, refer to M. J. Igunatius et al., Proc. Natl. Acad. Sci. U.S.A., 83, 1125 (1986)), which suggests that apolipoprotein E will play an important role in repairing nervous systems. Moreover, it has recently been reported that a remarkable reduction in a plasma cholesterol level can be observed by intravenous administration of apolipoprotein E to WHHL rabbit, which is a model animal for human familial hypercholesterolemia homozygote (Yamada et al., Proceeding of National Academy Science USA, Vol. 86, pp. 665-669, 1989). Also, it has been reported that plasma cholesterol and plasma triglyceride can be noticeably decreased by transducing a gene for apolipoprotein E into the mouse liver and expressing apolipoprotein E in a large mass (Shimano, H. et al., Journal of Clinical Investigation, Vol. 90, pp. 2084-2091, 1992).
As is apparent from these reports, the increase in plasma apolipoprotein E concentration has been regarded as extremely effective for the treatment of hyperlipemia, especially, familial hypercholesterolemia homozygote which has been hitherto considered as difficult to be treated with the prior art drugs.